COVID-19-associated multiple colonic perforations in a 6-month-old infant: a rare case report

Abstract

Background

While COVID-19 primarily manifests as a respiratory illness, gastrointestinal complications—including severe colitis and perforation—have been reported, particularly in adults. However, such presentations in infants remain exceedingly rare.

Case presentation

A 6-month-old infant presented with lethargy and poor feeding, initially diagnosed with sepsis. Subsequent testing confirmed COVID-19 positivity. During hospitalization, the patient developed feeding intolerance, vomiting, and abdominal distension. Imaging revealed free intraperitoneal fluid with suspected perforation. Emergency laparotomy revealed perforations in the transverse and descending colon, necessitating total colectomy.

Conclusion

This case provides laboratory and histopathological evidence linking SARS-CoV-2 to intestinal perforation in infants, suggesting that SARS-CoV-2 may contribute to ischemic or inflammatory bowel injury leading to perforation. Early surgical intervention is critical in such scenarios. Further research is needed to establish causality and pathophysiology.

Introduction

COVID-19, caused by SARS-CoV-2, is primarily characterized by respiratory involvement, yet its multisystemic effects increasingly underscore its complexity [1]. Among extrapulmonary manifestations, gastrointestinal (GI) complications—ranging from mild symptoms like diarrhea and vomiting to severe pathologies such as colitis and perforation—have gained recognition, particularly in adults. However, the pediatric population, especially infants, remains an underreported demographic for severe GI sequelae of COVID-19 [2].

The GI tract’s susceptibility to SARS-CoV-2 is biologically plausible due to the abundant expression of angiotensin-converting enzyme 2 (ACE-2) receptors in enterocytes, the primary viral entry point [3]. While GI symptoms occur in 10–20% of pediatric COVID-19 cases, life-threatening complications like intestinal perforation are exceptionally rare [4]. Existing literature on COVID-19-associated perforation predominantly describes adult patients [5], often attributing the phenomenon to virus-induced hyperinflammation, microthrombosis, or ischemic injury [6]. In contrast, reports in children are sparse, with only a handful of cases documented worldwide, none involving infants.

This gap in evidence raises critical questions about the mechanisms and risk factors for severe GI injury in young children. Infants, with their immature immune systems and distinct ACE-2 receptor distribution, may represent a vulnerable subgroup. Furthermore, the overlap between COVID-19-related abdominal pathology and more common neonatal conditions—such as necrotizing enterocolitis or sepsis—can delay diagnosis, exacerbating morbidity.

We present a novel case of a 6-month-old infant with COVID-19 who developed multifocal colonic perforations, necessitating emergent surgical intervention. This report aims to alert clinicians to the potential for catastrophic GI complications in pediatric COVID-19, advocate for early imaging in unexplained abdominal distress, and stimulate research into the underlying pathophysiology linking SARS-CoV-2 to intestinal necrosis in infants.

Case presentation

History and initial presentation

A previously healthy 6-month-old male infant presented to our tertiary care center with lethargy, poor feeding, and fever for two days. Initial evaluation suggested sepsis, and broad-spectrum antibiotics were initiated. RT-PCR confirmed SARS-CoV-2 infection.

Laboratory findings supporting COVID-19-associated pathology

The patient exhibited clear laboratory evidence of COVID-19-associated systemic complications, including marked hypercoagulability (elevated D-dimer and fibrinogen), cytokine storm (significantly elevated IL-6 and CRP), and thrombotic microangiopathy (prolonged PT/INR). Concurrent hepatic injury (AST/ALT > 10× upper limit) was observed, while negative blood cultures excluded secondary bacterial sepsis (see Table 1 for full laboratory parameters).

Table 1.

The infant’s laboratory tests

Test	Result	Reference Range	Interpretation
RT-PCR (COVID-19)	Positive	Negative	Confirmed infection
CRP	++	< 1 mg/dL	Strongly positive
D-Dimer	11,440 ng/mL	< 500 ng/mL	Elevated
Fibrinogen	644 mg/dL	200–400 mg/dL	Elevated
Ferritin	966,000 ng/mL	30–400 ng/mL	Significantly elevated
AST	1,670 U/L	10–40 U/L	Elevated
ALT	730 U/L	7–56 U/L	Elevated
ALK	230 U/L	44–147 U/L	Elevated
PT	30.1 s	11–13.5 s	Prolonged
PTT	51.1 s	25–35 s	Prolonged
INR	2.26	0.8–1.2	Elevated
WBC	23,000/µL	5,000–10,000/µL	Elevated
Lymphocytes	> 75%	20–40%	Increased proportion
Hemoglobin	7.7 g/dL	11–16 g/dL	Low
Hematocrit	25.5%	35–45%	Low
Platelets	519,000/µL	150,000–450,000/µL	Normal
Blood Culture	Negative	Negative	No bacterial growth
Interleukin	200 pg/mL	< 10 pg/mL	Elevated (cytokine storm)

Hospital course and deterioration

On day 3 of admission, the infant developed abdominal distension, bilious vomiting, and feeding intolerance. Abdominal imaging revealed compelling evidence of acute surgical pathology. Preoperative radiography and CT demonstrated pneumoperitoneum with free fluid accumulation in characteristic locations including Morrison’s pouch and the subdiaphragmatic region, accompanied by hyperdense changes in the mesenteric vasculature suggestive of thrombotic complications. Key CT features included:

• Significant free fluid in the right paracolic space, Morrison’s pouch, and subdiaphragmatic region.

• Absence of necrotizing enterocolitis (NEC) or mechanical obstruction (no pneumatosis intestinalis or transition point).

• Mesenteric vein hyperdensity indicating possible thrombotic microangiopathy.

The combination of pneumoperitoneum with these radiographic findings, in conjunction with the patient’s clinical deterioration, necessitated emergent surgical exploration for suspected perforation with fecal peritonitis.

Cytokine storm

The patient suddenly developed high fever, hypotension, and lethargy during hospitalization. Interleukin levels were reported at 200. Inotropic support was initiated, and the patient was placed on mechanical ventilation.

Operative findings

Laparotomy identified:

1. Multiple perforations in the transverse and descending colon.

2. A fistulous tract near the hepatic flexure.

3. Purulent peritonitis with fecal contamination Due to the extent of injury, a terminal colectomy with ileostomy was performed. Histopathology revealed focal transmural necrosis without vasculitis, raising suspicion of COVID-19-induced ischemic injury.

A total colectomy with ileostomy was performed, resecting the transverse colon, descending colon, and hepatic flexure fistula.

Postoperative outcome

The ileostomy was created to divert fecal flow, mitigate obstruction risk, and optimize nutritional status. Reversal is planned after 6 months pending bowel healing and nutritional recovery.

The infant recovered gradually with TPN support and was discharged on postoperative day 14. Follow-up at 3 months showed adequate weight gain and no further complications.

Discussion

The pathogenesis of COVID-19-associated intestinal perforation remains incompletely understood, though several mechanistic pathways emerge from existing evidence [7]. The temporal association between SARS-CoV-2 infection and colonic perforation, while not definitive proof of causation, presents a biologically plausible relationship given the absence of alternative etiologies (e.g., NEC, mechanical obstruction). The infant’s laboratory profile– including a hypercoagulable state (D-dimer: 11,440 ng/mL; fibrinogen: 644 mg/dL) and cytokine storm (IL-6 > 200 pg/mL)– mirrors established mechanisms of COVID-19-induced intestinal injury. Histopathological findings (transmural necrosis without vasculitis) further corroborate SARS-CoV-2 as a probable contributor rather than an incidental finding, consistent with current understanding of viral-mediated endothelial dysfunction and thromboinflammation.

Although transmural necrosis may suggest necrotizing enterocolitis (NEC), this case exhibits pathognomonic differences: (1) multifocal rather than diffuse colonic involvement, (2) no radiographic evidence of pneumatosis intestinalis, and (3) histopathological absence of NEC-defining features (vasculitis, submucosal edema). These distinctions, when contextualized with elevated COVID-19 biomarkers (D-dimer > 10× upper limit) and the patient’s virologic status, support a novel pattern of SARS-CoV-2-associated intestinal necrosis. This phenotype diverges from classical NEC pathogenesis, instead implicating direct viral cytopathic effects and/or COVID-19-specific microthrombotic mechanisms.

The virus’s affinity for ACE-2 receptors, densely expressed in intestinal epithelium, suggests potential direct cytopathic effects [8]. This aligns with histopathological findings in adult COVID-19 autopsies demonstrating viral RNA in enterocytes alongside apoptotic changes [9]. However, our patient’s multifocal perforations without diffuse mucosal necrosis argue against pure viral cytotoxicity as the sole explanation.

Mounting evidence implicates COVID-19-associated microthrombosis as a critical contributor. The virus’s well-documented prothrombotic state, mediated through endothelial activation, platelet hyperreactivity, and impaired fibrinolysis, may precipitate mesenteric microvascular occlusion [10]. Pediatric case series have identified elevated D-dimer and fibrinogen levels in severe COVID-19, mirroring the hypercoagulable profile observed in our infant [11]. This thrombotic predisposition could explain the segmental nature of ischemic injury seen intraoperatively, distinct from the pan-colonic involvement characteristic of NEC.

The cytokine storm phenomenon, while more commonly associated with pulmonary complications, may equally drive intestinal injury [12]. Elevated IL-6 and TNF-α levels, frequently observed in pediatric multisystem inflammatory syndrome (MIS-C), can compromise gut barrier integrity through tight junction disruption [13]. Our patient’s operative findings of serosal inflammation without frank necrosis support this inflammatory-mediated injury pattern. Notably, similar pathology has been described in coronavirus-infected animal models, where cytokine-driven increases in intestinal permeability preceded bacterial translocation.

The clinical implications of these findings are threefold. First, our case reinforces that infants COVID-19 may manifest primarily through severe GI pathology without preceding respiratory symptoms, challenging the traditional diagnostic paradigm. Second, the rapid progression from nonspecific symptoms to perforation underscores the necessity of early cross-sectional imaging in COVID-19-positive infants with abdominal distension, as ultrasound alone may miss early ischemic changes. Third, the presence of free air or clinical deterioration should prompt immediate surgical consultation, as delayed intervention risks catastrophic outcomes from fecal peritonitis.

These observations find support in emerging literature. A 2022 multicenter review identified 11 pediatric COVID-19 cases with GI perforation, 73% of whom lacked respiratory symptoms at presentation [14]. Similarly, a neonatal case series from Brazil documented COVID-19-associated pneumatosis intestinalis responsive to anticoagulation therapy, suggesting thrombotic microangiopathy as a unifying mechanism [15]. However, our case represents the first reported instance of multifocal colonic perforations in an infant, expanding the spectrum of COVID-19’s GI manifestations.

Therapeutic considerations remain controversial. While some authors advocate for early anticoagulation in suspected COVID-19-associated GI ischemia, the risk of hemorrhage in perforated cases necessitates caution [16, 17]. Our experience suggests that surgical resection remains the definitive treatment for established perforations, though adjuvant immunomodulatory therapy may merit exploration in select cases. Future research should focus on identifying biomarkers predictive of GI complications and elucidating whether viral variants differentially affect intestinal tropism.

Conclusion

This case underscores COVID-19 as a potential risk factor for life-threatening colonic perforation in infants. Clinicians should maintain a high index of suspicion for GI complications in pediatric COVID-19 cases, particularly those with unexplained abdominal distension or sepsis-like presentations. Further studies are needed to elucidate the pathophysiological link between SARS-CoV-2 and intestinal injury.

Abbreviations

SARS-CoV-2

Is the strain of coronavirus that causes COVID-19, a respiratory illness responsible for the COVID-19 pandemic

GI

Gastrointestinal

NEC

Necrotizing enterocolitis

ACE-2 receptors

Angiotensin-converting enzyme 2 receptors

Authors’ contributions

Credit authorship contribution statement: Ladan Teymoorzadeh: Writing– original draft, Validation, Investigation, Conceptualization. Ramez Nasiri: Writing– original draft, Validation, Investigation, Conceptualization. Ali Manafi Anari: Project Administration, Visualization, Validation, Investigation, Conceptualization. Sajjad Narimani: Writing– original draft, Validation, Investigation, Writing and Final editing of manuscript, Project Administration.

Funding

This work has not obtained any funding or grant support.

Data availability

The data will be made available upon request from the corresponding author.

Declarations

Ethics approval and consent to participate

Ethical approval was obtained from the Department of Pediatrics, Ali Asghar Children Hospital, Iran University of Medical Sciences.

Consent for publication

Informed consent for publication of clinical details was obtained from the parents of the patient.

Competing interests

The authors declare no competing interests.